A client who has asthma (a reactive airway disease) asks the nurse about the role of leukotrienes in this process. Leukotrienes have which immune response?
Produce the sensation of Itching.
Tighten airway and produce mucous.
Causes formation of bradykinin.
Serves as receptor for antigen.
The Correct Answer is B
Leukotrienes are inflammatory mediators derived from arachidonic acid metabolism, primarily produced by leukocytes (white blood cells) such as mast cells, eosinophils, and basophils. In the context of asthma, leukotrienes play a significant role in the pathophysiology of the disease by contributing to airway inflammation and bronchoconstriction. Here's a breakdown of their immune response:
A) Produce the sensation of itching:
Leukotrienes are not directly involved in producing the sensation of itching. Itching is often associated with histamine release rather than leukotrienes.
B) Tighten airway and produce mucous:
Correct. Leukotrienes are potent bronchoconstrictors that cause smooth muscle contraction in the airways, leading to narrowing (constriction) of the bronchioles. Additionally, they stimulate the secretion of mucus from goblet cells in the airway epithelium, contributing to airway obstruction and mucus production, which are characteristic features of asthma exacerbations.
C) Causes formation of bradykinin:
Bradykinin is a peptide mediator that is generated from the plasma protein kininogen and is involved in vasodilation, pain sensation, and inflammation. Leukotrienes are not directly responsible for the formation of bradykinin.
D) Serves as a receptor for antigen:
Leukotrienes do not serve as receptors for antigens. Instead, they are lipid mediators released in response to various stimuli, including allergens, infections, and irritants, and they act on specific receptors (e.g., leukotriene receptors) to exert their effects, such as bronchoconstriction and inflammation
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is A
Explanation
A) The usual types of reactions are mediated by antibodies:
Correct. Types I, II, and III hypersensitivity reactions are mediated by antibodies (IgE, IgG, or IgM) that bind to antigens and trigger immune responses. In contrast, Type IV hypersensitivity reactions are T-cell mediated and do not involve antibodies.
B) B-lymphocytes produce the offending substances:
This statement is incorrect. B-lymphocytes are involved in antibody-mediated immune responses (types I, II, and III hypersensitivity reactions), not Type IV hypersensitivity reactions, which are primarily mediated by T-lymphocytes.
C) They typically occur with the first exposure to an antigen:
This statement is incorrect. Type IV hypersensitivity reactions usually require sensitization upon initial exposure to an antigen, and subsequent exposures elicit the delayed hypersensitivity response. This is similar to types I, II, and III hypersensitivity reactions, which also involve sensitization upon initial exposure.
D) Delayed reactions are characterized by cytokine release:
This statement is partially correct. Type IV hypersensitivity reactions are characterized by a delayed onset (typically 24 to 72 hours after exposure) and involve the release of cytokines from activated T-lymphocytes, leading to inflammation and tissue damage. However, other types of hypersensitivity reactions may also involve cytokine release, so this feature alone does not differentiate Type IV from other types of reactions.
Correct Answer is C
Explanation
A) An increase in afterload results in decreased systolic pressure, which creates a decreased cardiac output:
This statement is not consistent with the Frank-Starling law. Afterload refers to the resistance against which the heart must pump blood during systole. An increase in afterload typically results in increased systolic pressure, not decreased, as the heart works harder to overcome the increased resistance. However, increased afterload can lead to decreased cardiac output due to the increased work of the heart.
B) A decrease in afterload causes the cardiac muscles to hypertrophy, resulting in increased diastolic volume:
This statement is not consistent with the Frank-Starling law. Afterload refers to the pressure or resistance against which the heart must pump blood during systole. A decrease in afterload typically reduces the workload on the heart, which may lead to reverse remodeling and a reduction in cardiac hypertrophy. Increased diastolic volume may occur due to reduced afterload, but it's not the direct result of hypertrophy.
C) An increase in preload results in greater shortening of myocardial fibers, thereby increasing contractility:
Correct. According to the Frank-Starling law, an increase in preload (end-diastolic volume or stretch of myocardial fibers) leads to greater overlap of actin and myosin filaments within myocardial fibers during systole. This increased overlap results in stronger myocardial contraction (increased contractility), leading to an increased stroke volume and cardiac output.
D) A decrease in preload results in increasing diastolic muscle fiber length, which impedes contractility:
This statement is not consistent with the Frank-Starling law. Preload refers to the degree of stretch of the myocardial fibers at the end of diastole. A decrease in preload would lead to decreased stretch of the myocardial fibers, not increasing diastolic muscle fiber length. Decreased preload typically results in decreased contractility rather than impediment to contractility due to reduced myocardial stretch.
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